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Biomedical subjects

M Anapliotou

Publications and source records attributed to M Anapliotou.

11 recordsLinked to original sources
PubMed2004

Estrogen receptor alpha gene analysis in osteoporosis and familial osteoporosis.

Estrogens are important determinants of bone mineral density (BMD) mediating their effects via estrogen receptor alpha (ERalpha) and beta (ERbeta). The strong genetic predisposition to osteoporosis, and the fact that alterations in the aminoterminal region of ERalpha have been linked to bone disturbances, prompted us to identify genetic alterations in exon 1 and exon 2 of ERalpha in osteoporotic individuals. Sixty-two unrelated normal subjects (age 46.1+/-9.5 years) and 72 unrelated osteoporotic subjects (age 52.3+/-7.9 years) were studied. Their menopausal status was pre- and perimenopausal. We also included 30 related osteoporotic individuals (mother-daughter or sister-sister relationship) (age 46.2+/-12.8 years) belonging to 14 families who where also pre- and perimenopausal. DNA was extracted from peripheral blood, exons 1 and 2 were amplified by polymerase chain reaction (PCR) and were further submitted to denaturing gradient gel electrophoresis (DGGE), single stranded conformational polymorphism (SSCP), restriction fragment length polymorphism (RFLP) and sequence analysis. Bone turnover markers were also determined. Two polymorphisms were identified in exon 1 (codons 10 and 87) in both normal and osteoporotic women. Statistical analysis revealed no difference (P>0.05) in the ERalpha genotype frequencies within osteoporotic families as compared with the same genotypes in the unrelated normal or osteoporotic subjects. Codon 10, codon 87 polymorphisms were not related to BMD or bone turnover markers. No other mutations were found in exons 1 and 2 in all subjects studied. Genetic alterations in exons 1 and 2 of ERalpha are not associated to osteoporosis and familial osteoporosis. Moreover, the codon 10 and codon 87 polymorphisms do not seem to be correlated with BMD and bone turnover markers.

Adult↗
PubMed2004

Presence of systemic autoimmune disorders in patients with autoimmune thyroid diseases.

OBJECTIVE: To evaluate the prevalence of antinuclear antibodies (ANA) in patients with autoimmune thyroid diseases (ATD) and the presence of systemic autoimmune disorders among ANA positive patients with ATD. METHODS: 168 consecutive patients with ATD with positive antithyroid antibodies and 75 healthy subjects were tested for the presence of ANA. ANA positive patients were further evaluated by complete history, physical examination, blood and urine tests, and immunological studies. Patients with subjective xerophthalmia and xerostomia were examined by objective tests. RESULTS: 58/168 (35%) patients with ATD were ANA positive compared with 7/75 (9%) healthy controls (p = 0.001). Of 58 ANA positive patients, 6 (10%) had anti-Ro antibodies, 1 had anti-Ro and anti-La antibodies, 7 (12%) had anti-dsDNA antibodies, and 7 (12%) had medium levels of IgG and/or IgM anticardiolipin antibodies (aCL). No healthy subjects had positive anti-dsDNA, antibodies against the extractable nuclear antigens, or aCL. 5/58 (9%) patients fulfilled the criteria for Sjögren's syndrome (SS). Two patients had features related to systemic lupus erythematosus. No healthy subjects had clinical or laboratory characteristics of systemic autoimmune disorders. CONCLUSION: ANA are detected in 1/3 of patients with ATD. Anti-dsDNA, anti-Ro, and aCL can also be found in ANA positive patients with ATD. SS occurs in about 1/10 of ANA positive patients with ATD.

Adult↗
PubMed1999

The contribution of vitamin D receptor gene polymorphisms in osteoporosis and familial osteoporosis.

It is well established that genetic factors play a major role in the pathogenesis of osteoporosis. Previous reports have suggested that vitamin D receptor (VDR) gene polymorphisms, particularly the BB, tt and AA genotypes, are associated with low bone mineral density (BMD). If these VDR genotypes are indeed an important determinant of BMD, then a population of related osteoporotic individuals (mother-daughter or sister-sister relationship) should have a high prevalence of the BB, tt or AA VDR genotypes. To test this hypothesis we determined the VDR genotypes in 26 osteoporotic persons (age 44.3 +/- 12.7 years, mean +/- SD) belonging to 12 families. Furthermore, for comparison with existing studies, we applied the VDR genotype analysis in a population of 53 unrelated healthy subjects (age 45.2 +/- 9.8 years, mean +/- SD) and 59 unrelated osteoporotic subjects (age 52.1 +/- 9.0 years, mean +/- SD). The menopausal status of the healthy and osteoporotic populations was pre-, peri- and mostly early postmenopausal. The proportions of the three genotypes, BB, tt and AA, within the 12 osteoporotic families were 15%, 12% and 27%, respectively, whereas the proportions of the other three homozygous genotypes (bb, TT, aa) were 50%, 50% and 23%. The distribution of the BB, tt and AA genotypes in the normal population was 21%, 21% and 36%, respectively (vs bb, TT, aa: 36%, 38%, 21%), whereas in the osteoporotic population it was 24%, 20% and 34% (vs bb, TT, aa: 27%, 34%, 14%). Our data indicate that there is not a statistically significant (p>0.05) difference in the VDR genotype frequencies within osteoporotic families as compared with the same genotypes in the population of unrelated normal or osteoporotic subjects. VDR genotype analysis showed no significant relation between VDR polymorphisms and BMD or Z-score values at the lumbar spine. This study demonstrates the lack of a heritability pattern between the BB, tt and AA genotypes and low BMD.

Adult↗
PubMed1997

Sex hormone levels in the serum of patients with pancreatic adenocarcinoma.

The objective of this study was to evaluate the levels of several pituitary and gonadal hormones in pancreatic adenocarcinoma. We examined circulating levels of LH, FSH, Testosterone, Oestradiol, Progesterone and delta 4-Androstenedione in 36 patients with pancreatic adenocarcinoma, 12 patients with chronic pancreatitis and 87 age matched controls. According to our findings males with pancreatic cancer were found to have higher levels of FSH (p < 0.01). LH and oestradiol (p < 0.001) and lower levels of progesterone (p < 0.01) and testosterone (p < 0.05) than the controls. Female patients with pancreatic cancer were found to have higher levels of oestradiol (p < 0.001) and lower levels of LH, FSH and progesterone (p < 0.001), compared with group of healthy volunteers. Our data provide evidence of a generalised dysfunction of the hypothalamic-hypophysial-gonadal axis in pancreatic cancer patients.

Adenocarcinoma↗
PubMed1995

Effect of testosterone administration, pre- and postnatally, on the immune system of rats.

This study was undertaken to investigate and compare in vitro and in vivo immune parameters between female and male rats. We analysed the T-cell proliferative responses to syngeneic and allogeneic cellular antigens (syngeneic and allogeneic mixed lymphocyte reaction), as well as the IgG levels in the sera of our study groups. It has also been studied the influence of gonadectomy and the effect of testosterone administration pre- and postnatally on the above parameters. Our findings showed that hormonal manipulations, can alter the differences observed in immune response between female and male rats. In addition, it is demonstrated that pre- and postnatal sexual steroid manipulations could provoke long lasting immunological effects.

Animals↗
PubMed1981

Heterogeneity of prolactin responses to oestradiol benzoate in women with prolactinomas.

Serum prolactin concentrations were measured for 72 h after intramuscular injection of 1 mg of oestradiol benzoate in six normoprolactinaemic women and nineteen with a prolactinoma (eleven with an obviously enlarged pituitary fossa and eight with a normal pituitary fossa). The group with an obvious tumour showed a rise in mean serum prolactin at 48 h to 122% of basal concentrations (p less than 0.05), and at 72 h to 137% of basal concentrations (p less than 0.01). Individual responses were variable, but in four patients serum prolactin rose to 165% or more of basal concentrations. In the group with a prolactinoma and a normal pituitary fossa serum prolactin at 72 h was 121% of basal concentrations (p less than 0.05). Normoprolactinaemic women showed no significant change in serum prolactin at any time. This study demonstrated a heterogeneity of serum prolactin responses to acute oestradiol administration in women with prolactinomas. Some patients with large tumours had a hypersensitive response to oestradiol. This heterogeneity of response could account for the present unpredictability of expansion of prolactinomas during pregnancy.

Adolescent↗
PubMed1981

Results of three-times-per-week long-term administration of a luteinizing hormone-releasing hormone (LHRH) analog, D-Ser-(TBU)6-LHRH-(EA)10 in primary amenorrhea.

The effectiveness of a luteinizing hormone (LH)-releasing hormone (LHRH) analog, D-Ser-(TBU)6-LHRH-(EA)10 (Hoe 766), applied intranasally in a 3 days-per-week regimen, was assessed in four patients with hypogonadotropic or normogonadotropic primary amenorrhea by measuring LH, follicle-stimulating hormone (FSH), and estradiol (E2) levels before and 4 hours after its application and by observing the clinical effects of these hormones on the genital tract. The LH response increased progressively over the first 21 days (nine applications) in three of the four patients; it was subsequently reduced but never abolished throughout the study, which was terminated with the 25th application on the 59th day. Basal values of E2 increased until the 12th to 14th day (fifth or sixth application) and then showed a definite decline despite the continuing increase in LH response. FSH release attained a maximum by the second to fourth application and its magnitude of response remained remarkably stable thereafter. The clinical response did not correspond to the serum levels of E2. It is postulated that the development of LH unresponsiveness is due to desensitization of the receptors by the analog. The poor response of the genital tissues to the normal levels of E2 and the subsequent decrease in E2 levels, which occurred despite increasing LH responsiveness, are attributed to an inhibitory action of the analog on E2 biosynthesis in the ovary and on E2 receptors in the genital organs.

Adult↗
PubMed1981

Prolactin and placental hormone levels during pregnancy in prolactinomas.

Prolactin (PRL) and the placental hormones, estradiol (E2), estriol (E3), progesterone (PG), chorionic gonadotropin (HCG), and placental lactogen (HPL) were serially measured throughout pregnancy and early postpartum in three patients with prolactinomas in whom pregnancy was achieved by one of the three modalities of treatment: bromocriptine administration (patient I), irradiation of the pituitary (patient II), and human gonadotropin administration after excision of the adenoma (patient III). It was found that PRL in patient I reached the high pretreatment levels in the 2nd month of pregnancy and increased to further abnormal concentrations in the last 2 months, but fell at the onset of labor 1 week after an episode of severe headache. The PRL changes in this patient were attributed successively to tumor expansion and apoplexy. In patient II PRL decreased after irradiation, but was not normalized. During pregnancy it remained moderately increased presenting minor fluctuations. The third patient with postoperative GH and TSH pituitary insufficiency had low pretreatment PRL levels which remained practically unchanged throughout pregnancy. The two last patients gave birth to identical twins. The placental hormones were found normal in all three patients but E2 and PG were relatively increased during the last weeks of pregnancy in the twin pregnancies. Amniotic fluid and umbilical cord PRL and E2 concentrations were normal. The patients presented agalactia and suckling did not induce a PRL increase. We conclude that a) serial PRL measurements during pregnancy reflect the changes occurring in the prolactinomas and are essential in monitoring the patients bearing these tumors; b) maternal hyperprolactinemia or failure of PRL to increase during pregnancy do not influence either the secretion of placental hormones or PRL concentration in amniotic fluid and the newborn; and c) hyperprolactinemia during pregnancy is of maternal pituitary origin.

Adenoma↗